Evidence map›Paper›PMID 30668549›Full record

ArticleJCI insight2019

Human antigen R as a therapeutic target in pathological cardiac hypertrophy.

Lisa C Green, Sarah R Anthony, Samuel Slone, Lindsey Lanzillotta, Michelle L Nieman, Xiaoqing Wu, Nathan Robbins, Shannon M Jones, Sudeshna Roy, A Phillip Owens and 7 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. HuR Regulates GATA3-Driven Type 2 Inflammation in CD4bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. HuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Article
  8. Review
  9. HuR ablation destabilizesFrontiers in immunology · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. RNA binding proteins as mediators of pathological cardiac remodeling.Frontiers in cell and developmental biology · 2024
    Review
  19. Single-cell analysis reveals lysyl oxidase (Lox)Journal of advanced research · 2023
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 5 institutions in 1 country.

Lisa C GreenDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
Sarah R AnthonyDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
Samuel SloneDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
Lindsey LanzillottaDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
Michelle L NiemanDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Xiaoqing WuDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.
Nathan RobbinsDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
Shannon M JonesDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
Sudeshna RoyDivision of Chemical Biology and Medicinal Chemistry, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina, USA.
A Phillip OwensDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
Jeffrey AubeDivision of Chemical Biology and Medicinal Chemistry, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina, USA.
Liang XuDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.
John N LorenzDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Burns C BlaxallDepartment of Pediatrics, Division of Molecular Cardiovascular Biology, Heart Institute, Cincinnati Children's Hospital Medical Center (CCHMC), Cincinnati, Ohio, USA.
Jack RubinsteinDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
Joshua B BenoitDepartment of Biological Sciences, University of Cincinnati, Cincinnati, Ohio, USA.
Michael TranterDepartment of Internal Medicine, Division of Cardiovascular Health and Disease and.
University of Cincinnati Medical Center · USUniversity of Kansas · USUniversity of North Carolina at Chapel Hill · USCincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

Molecular cancer therapy targeting HuR-ARE interactionR01CA191785 · NCI · UNIVERSITY OF KANSAS LAWRENCE · PI AUBE, JEFFREY, XU, LIANG · 2015 to 2019
$2.1M
Investigation of Human Antigen R (HuR) as a Novel Mediator of Cardiac HypertrophyR01HL132111 · NHLBI · UNIVERSITY OF CINCINNATI · PI TRANTER, MICHAEL · 2016 to 2020
$1.8M
Small molecules modulating RNA-binding protein Msi1R01CA178831 · NCI · UNIVERSITY OF KANSAS LAWRENCE · PI NEUFELD, KRISTI L, XU, LIANG · 2014 to 2016
$1.3M
NCI NIH HHS R01 CA178831NCI NIH HHS R01 CA191785NHLBI NIH HHS R01 HL132111
6 · The paper itself

Abstract

RNA binding proteins represent an emerging class of proteins with a role in cardiac dysfunction. We show that activation of the RNA binding protein human antigen R (HuR) is increased in the failing human heart. To determine the functional role of HuR in pathological cardiac hypertrophy, we created an inducible cardiomyocyte-specific HuR-deletion mouse and showed that HuR deletion reduces left ventricular hypertrophy, dilation, and fibrosis while preserving cardiac function in a transverse aortic constriction (TAC) model of pressure overload-induced hypertrophy. Assessment of HuR-dependent changes in global gene expression suggests that the mechanistic basis for this protection occurs through a reduction in fibrotic signaling, specifically through a reduction in TGF-β (Tgfb) expression. Finally, pharmacological inhibition of HuR at a clinically relevant time point following the initial development of pathological hypertrophy after TAC also yielded a significant reduction in pathological progression, as marked by a reduction in hypertrophy, dilation, and fibrosis and preserved function. In summary, this study demonstrates a functional role for HuR in the progression of pressure overload-induced cardiac hypertrophy and establishes HuR inhibition as a viable therapeutic approach for pathological cardiac hypertrophy and heart failure.

Indexed as

AnimalsCardiotonic AgentsDisease Models, AnimalELAV-Like Protein 1FibrosisHeart FailureHeart VentriclesHumansHypertrophy, Left VentricularMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumMyocytes, CardiacRNA-SeqCardiotonic AgentsELAVL1 protein, humanElavl1 protein, mouseELAV-Like Protein 1CardiologyCardiovascular diseaseCell Biology

Identifiers

PMID30668549
PMCPMC6478406
OpenAlexW2911847768

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.